Abstract:
:Reduced lymphopoiesis during aging contributes to declines in immunity, but little consideration has been given to its effect on the development of hematologic disease. This report demonstrates that age-related defects in lymphopoiesis underlie the myeloid dominance of adult leukemia. Using a murine model of chronic myeloid leukemia, an adult-onset malignancy that arises from transformation of hematopoietic stem cells by the BCR-ABL(P210) oncogene, we demonstrate that young bone marrow (BM) cells that were transformed with BCR-ABL(P210) initiated both a myeloproliferative disorder (MPD) and B-lymphoid leukemia, whereas BCR-ABL(P210)-transformed old BM cells recapitulated the human disease by inducing an MPD with rare lymphoid involvement. In addition, the lesser severity of MPDs initiated from old BCR-ABL(P210)-transduced BM cells revealed unappreciated defects in aged myeloid progenitors. These data demonstrate that aging affects patterns of leukemogenesis and indicate that the effects of senescence on hematopoiesis are more extensive than previously appreciated.
journal_name
Bloodjournal_title
Bloodauthors
Signer RA,Montecino-Rodriguez E,Witte ON,McLaughlin J,Dorshkind Kdoi
10.1182/blood-2007-01-069401subject
Has Abstractpub_date
2007-09-15 00:00:00pages
1831-9issue
6eissn
0006-4971issn
1528-0020pii
blood-2007-01-069401journal_volume
110pub_type
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